Table of Contents

HYPERCALCEMIA................................................................................................................................................. 1
HEMODIALYSIS...............................................................................................................................................................3
VOLUME EXPANSION WITH NS..........................................................................................................................................3
LOOP DIURETICS..............................................................................................................................................................3
HYPOCALCEMIA.................................................................................................................................................. 3
HYPERPHOSPHATEMIA....................................................................................................................................... 6
PHOSPHATE BINDERS.......................................................................................................................................................7
CALCIUM.......................................................................................................................................................................7
HYPOPHOSPHATEMIA......................................................................................................................................... 7

Calcium
Serum calcium
 Total (bound + free): 8.5 – 10.5 mg/dL
o Measures calcium found in ECF
o Affected by hypoalbuminemia
o Affected by changes in calcium binding to albumin
 metabolic alkalosis – fraction bound to albumin ↑
 Ionized (free): 4.5 – 5.4 mg/dL
o Active form
o Maintained in tight range
 Corrected calcium equation
o Serum calcium (mg/dL)
o Serum albumin (g/dL)
Corrected Ca=measured Ca+0.8(4−serum albumin)
o Avoid this equation in critically ill patients (measure ionized calcium)

Hypercalcemia
Total serum calcium >10.5 mg/dL

 3 mechanisms
o ↑ Bone resorption
o ↑ GI absorption
o ↑ tubular Reabsorption in the kidneys
 ↑ serum Phosphorous ↓ Ca
o ↑ PTH
 Bone: ↑ osteoclast, ↑ osteoblast activity in bone - ↑ Ca mobilization
  Kidney:
 ↑ renal calcium reabsorption, ↓ renal phosphorous reabsorption
o  ↑ serum Calcium  ↑ calcitonin (turns off process)
 ↑ renal activation of 1,25-(OH)2 D3
o  GI tract: ↑ intestinal Ca and phosphorous absorption
  ↑ serum Calcium  ↑ calcitonin (turns off
process)
 Causes
o Cancers
o Hyper-PTH
o Medications
o Granulomatous diseases
o Endocrine diseases
o Others
 Drug-induced hypercalcemia
o Thiazides
o Lithium
o Vitamin D
o Calcium
o Vitamin A
o Aluminum/Magnesium antacids
o Theophylline
o Tamoxifen
o Ganciclovir
 Presentation
o Depends on severity and acuity
o Mild – to – moderate (Ca <13 mg/dL):
 may be asymptomatic
 fatigue, weakness
o acute (d/t cancer)
 anorexia
 n/v
 constipation
 polyuria
 polydipsia
 nocturia
o Hypercalcemic crisis (Ca>15 mg/dL)
 Patient may be unarousable
 AKI
 Coma
 Arrhythmia
 Death
o Chronic hypercalcemia
  Soft tissue calcification
 Hypercalciuria
 Interstitial nephrocalcinosis leading to CKD
 Nephrolithiasis
 ↑ Ca + ↑P + ↑ PTH = deposition
 Treatment
o Acute hypercalcemia with EKG changes/neurological effects/ pancreatitis
 Treat rapidly
 Loop diuretic + hydration: drop 2-3 mg/dL over 1-2 days

Hemodialysis
 For severely reduced kidney function: low to no calcium bath (dialysis solution) – steep
concentration gradient
 Loop diuretics won’t work
Volume expansion with NS
 Mechanism
o ↑ natriuresis
o ↑ urinary calcium excretion
 May need to add electrolytes after initial hydration (if using loop diuretic)
o Potassium
o Magnesium
Loop diuretics
 Furosemide
 Torsemide
 Bumetanide
 Ethacrynic acid
 Mechanism
o Block Ca and Na reabsorption in thick ascending limb
o ↑ urinary calcium excretion
 Caution – DO NOT DEHYDRATE PATIENT
o ↑ calcium reabsorption in PCT
 Monitor
o Fluid status
o K
o Mg

Hypocalcemia
Total calcium <8.5 mg/dL, ionized calcium <4.4 mg/dL ↓ Ca, ↑ PTH
 High prevalence in ICU (hypoalbuminemia)
 Generally, not medical emergency in most cases
o Emergent treatment warranted if seizures or tetany
 Generally, PTH is elevated
o Exceptions: hypo-PTH, hypomagnesemia
 Causes
o Vitamin D deficiency
 Active vitamin D (1,25-(OH)2 D) essential for absorption of Ca and P in the
gut
 Leads to chronic hypocalcemia
 Causes
 Malnourished populations – milk fortification
 GI disease or surgery
 CKD (inability to activate vitamin D)
o Hypomagnesemia
 ↓ Mg 
 Impaired PTH secretion
 Leads to PTH resistance in target organs
 May lead to severe, symptomatic hypocalcemia
 If present, patient will be unresponsive to calcium replacement
 Replete magnesium first!
o Hungry bone syndrome
 Follows parathyroidectomy/thyroidectomy
 Transient response post surgery
 Calcium ↓ rapidly
 Treatment: calcium replacement and frequent monitoring
 Monitor q6h x 1-2 days
o Hypo-PTH
 May be asymptomatic
o Medications
 Furosemide
 Cinacalcet
 Phosphorous (PO)
 Bisphosphonates… ( major ones)
 Clinical presentation
o Varies based on acuity
o Neuromuscular
 Paresthesia especially around mouth
 Cramping
 Tetany
 Laryngeal spasm
o CNS
 Depression, anxiety
 Seizure
 Confusion
 Hallucination
  Memory loss
o Dermatologic
 Alopecia
 Changes in nails
o Cardiac
 Prolonged QTc
 Symptoms similar to CHF
 Arrhythmia
 Bradycardia
 Hypotension
 Physical exam findings
o + Chvostek’s sign – facial twitching while tapping facial nerve
o + Trousseau’s sign – carpal spasm when BP cuff inflated >SBPx3 min

Phosphorous
Serum phosphorous: 2.5 – 4.5 mg/dL

 Phosphorous is essential for numerous biological processes

o Normal cell function
o Metabolism
o Enzymatic reactions
o Oxygen delivery to tissues
o ATP
 Absorption
o Gut
o Increased by
 Active vitamin D (1,25-(OH)2 D3)
 PTH
 Low phosphorous diet
o Decreased by
 High dietary intake of phosphorous and magnesium
 Glucocorticoids
 hypoPTH
 Renal excretion
o glomerular filtration
o Proximal tubular reabsorption
 Normally 85-90% reabsorbed
 PTH inhibits reabsorption
 1,25(OH)2 D3 enhances absorption in PCT
 FGF231 inhibits reabsorption
1
FGF23 = fibroblast growth factor 23
  Regulates phosphorous homeostasis
o ↓ tubular reabsorption in kidney (↑ phosphaturia)
o Inhibit 1-α-hydroxylase (activates vitamin D  no active
vitamin D  no absorption of P in PCT)

Hyperphosphatemia
Serum phosphorous >4.5 mg/dL

 Causes
o Renal impairment
o Iatrogenic
o Rapid tissue breakdown (rhabdomyolysis)
o Acid-based (Lactic acidosis, DKA)
 Ca/P precipitation, soft tissue deposition
o Acute:
 Intrarenal calcification
 Nephrolithiasis
 Obstructive uropathy
o Chronic:
 Eye, skin, heart, vessels, lung, GI…
 Signs and symptoms
o n/v/d, lethargy, seizure
o hypocalcemia
 Treatment:
Phosphate binders
 Bind phosphorus in the gut
 Mostly for chronic treatment/prevention
Calcium
 Treats emergent hyperphosphatemia leading to hypocalcemia

Hypophosphatemia
Mild: serum phosphorous 1-2 mg/dL (usually asymptomati c)
Severe: Serum phosphorous <1 mg/dL (usually asymptomati c)

- Life threatening
- Metabolic encephalopathy (irritability  weakness  paresthesia, numbness 
confusion  seizures  coma)
- Skeletal dysfunction, rhabdomyolysis
- Others – cardiomyopathy, hemolysis

 Incidence in critically ill ~20-30%

 Causes
 o GI (↓ absorption)
 Alcoholism
 Medications (cations)
o Kidney (↓ absorption)
o Redistribution (Shifts to intracellular)
 Important cause of severe hypophosphatemia
 Associated with refeading/hyperalimentation and recovery
 Acute hypophosphatemia
o Glucose induces insulin secretion, causes phosphorous to
move from extracellular to intracellular
 Gradual hypophosphatemia (over ~1 week)
o Tissue repair
o Hungry bone
o Respiratory alkalosis
o During DKA treatment and recovery
o Medications: glucose, insulin, hormones, steroids
o Alcoholism
 Prevention and treatment
o Recognize risk factors
 Alcoholism
 DKA
 TPN (addition of phosphorous important)
o IV phosphate replacement for severe/symptomatic
 Risks are hypocalcemia, soft-tissue deposition
 Hypomagnesemia
 Based on product: may see hyperkalemia or hypernatremia
o PO phosphate replacement for mild-moderate/asymptomatic